The Missing Link Between LDL & Atherosclerosis | Episode 45
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- Опубліковано 23 лип 2023
- LDL-cholesterol--usually cast as the villain in the disease process of atherosclerosis. But is cholesterol the main problem? Why does your doctor want to lower the level of LDL as much as possible?
Then there are others who say that high LDL levels are not the problem, it's mainly inflammation we should worry about. Just lower your inflammation and you should be fine.
This episode will discuss the link between LDL, atherosclerosis/heart disease and inflammation. This is the MISSING LINK that has been right in front of our eyes. Make sure you don't miss this episode.
#atherosclerosis #LDL #lipoproteins #heartdisease #reversedisease #metabolichealth #statins #cholesterol
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BS
@HowardDoss-ij2me Thank you for taking the time to listen and to give your opinion. I thought I would share the following articles for your consideration:
1) This first one is a news report on some latest research: www.news-medical.net/news/20230227/Study-supports-the-concept-of-atherosclerosis-as-a-T-cell-autoimmune-disease-targeting-the-arterial-wall.aspx
2) www.ncbi.nlm.nih.gov/pmc/articles/PMC3984678/#:~:text=Giving%20the%20similarities%20with%20autoimmune,early%20stages%20of%20the%20disease.
3) www.nature.com/articles/s44161-023-00230-0
I'd be sincerely interested in hearing your feedback and critique of those studies. This is how real science is done so I appreciate your opening up the discussion. This is the thoughtful, well-considered conversation that I've been trying to stimulate and I am grateful for your succinct remark. I've pinned your comment so others can follow and participate. Thank you again!
Warmly,
Dr. Loh
Another thought provoking episode. The antigen angle is very interesting indeed. Thanks, Dr. Loh! 🙏🏽
Thank you, Mr. Blue. I had one eye on the clock the whole time--stressful!
Please look at Dr Malcolm Kendrick's book "the clot thickens", I'd love to hear your thoughts on his theory of the development of atherosclerosis.
@ogeoge6000 I'd be happy to do that. I was just finalizing topics for my series on Atherosclerosis which will come out in subsequent weeks and your request will be included. My aim in doing this series on Atherosclerosis is to tie up loose ends, debunk myths and help people understand the true origins (and risks) of this disease.
The subject is extremely complex and I can understand the need to simplify things but often this is at the expense of clarity and understanding. My own weakness has been trying to put in large chunks of detail in each episode, so now I'm trying to cut the detail and spread things out over a few episodes for better digestibility. In any case, I was not going to address the clot much since it seemed obvious but I see that there is room for explanation here as well, so I am indebted to you for pointing that out, thank you.
@@vlmdrounds Thank you very much, I'm looking forward to all your videos on this subject.
Are you seeing the evidence from the Lean Mass Hyper-Responder (LMHR) studies?
Dave Feldman, Nick Norwitz PHD, Dr. William Cromwell.
I look at a LDL-cholesterol/apolipoprotein B ratio of 1.52 as good (at this time)
I'm afraid I haven't been following the studies you mentioned. Maybe when I have a bigger team one day. Right now it's a bit of a juggling act trying to do everything on my own!
@@vlmdrounds Understood. I don't have the background that you do, so I have the luxury of glossing over some of the details. With the US healthcare establishment failing me, I am just attempting to navigate the better signals amongst the noise.
It is refreshing to learn that the science isn't settled - but that we are fearfully and wonderfully made!
Each of the scientists I mentioned have YT channels - a suggestion for critiques in future videos?
@@jamesalles139 Thank you. I am sorry that you have had to be under the current sick care system. My dream is that there be a real, science-based alternative for everyone one day!
@@vlmdrounds Oh my and LoL I felt bad saying that you weren't a in another post, and figured I really ought to do some research to see if I knew what I was talking about. Dr. Loh, you don't go overboard 'tooting your own horn' on this YT platform.
And guess who I stumbled on. A patient. On Metabolic Multiplier.
_Love a conversation that heals: Dr. Vyvyane Loh_
BY NICHOLAS NORWITZ · PUBLISHED OCTOBER 8, 2020 · UPDATED DECEMBER 27, 2022
I am beside myself, having pretty much stepped in it.
speechless, I am going to get my dinner.
It is nice when the world gets smaller.
I have said this for ages
Saturated fats are extremely important. Cholesterol is also very important.. essential for life. LDLs can be good and can be bad. The process of turning good LDL into Bad LDL isnt driven by fat in the diet..its driven by carbohydrates. Sugars..enter the circulation and damage the LDL particles. VLDLs..then IDLs..then LDL..all have an apo b 100 marker on their surface. The LDL receptor binding site is crucial for the liver to accept and recognise an LDL particle..ITs sugar from both simple and complex carbs that damage these binding sites through a process called glycation. This stops the liver from recognising it. It also fractionally shrinks it..causing it to be termed as small LDLs. This leads to oxidation of the LDL particle. Sugar can also cause it to become glyco oxidised which causes oxidative stress to the liver which leads to fatty liver disease. This damages the apob100 protein..makes it impossible for the liver to remove it from the circulatory system. So in effect it accumulates in the blood. This is what we term as an increase LDL particle count. Its the particle count which is a much better predictor of cardio vascular risk. So for an oxidised LDL particle to enter into an atherosclerotic plaque it has to pass through the lining of the artery. It firstly needs to breach this brush like layer called the glycocalyx. High levels of blood sugar damage the glycocalyx. Lectins in foods also damage the glycocalyx. The loosening of the tight junction proteins holding the epithelial tissue together. This lets the oxidised LDLs and circulating monocytes to enter into the sub endothelial space. Once there these monocytes turn into a macrophage. These macrophages express scavenger receptors which can recognise and bind to the damaged LDL particles that the liver receptors could not. These engulfed macrophages leads to the formation of a foam cell..a macrophage packed with lipids. Its these foam cells that are contained within atherosclerotic plaque..end result a BLOCKAGE. This is process...remembering that SUGAR is the cause not FAT. Humans do not need to ingest a single gram of sugar..not a single gram...we can make all the necessary glucose from a process known as gluconeogenesis. So eating saturated fats will increase your LDL levels but its the SUGAR that makes it go bad. So make sure you understand this.and spread the word to everyone else who bad mouths cholesterol and LDLs. They are crucial for life.
As a medic Meta analysis studies have shown the higher LDLs in your body..the longer you LIVED.
Yeah that’s most definitely not what she said lol.
You’re getting better at being more concise. Now just talk a little faster and you’ll shave another ten minutes off the video length 😜
But seriously, nice job covering a super complex topic. Wondering if you can dive into the pros and cons of various therapies (statins, Ezetimibe, natural remedies like psyllium, etc) would be interesting to hear your take.
Pfff, I was trying to talk fast but not so fast as to be incomprehensible, one eye on the clock, trying to remember my notes.....quite exhausting! I had told my friends it would be 30 mins and was a bit disappointed when I clocked in at 35 mins!
And yes, super complex--I had to leave out a bunch of stuff but hopefully it hit the main points. I'd like to hone in on some details in future episodes and then get to your suggestion of talking about the therapies. 👍
And let me practise speed-talking a bit more in the meanwhile....!😁
@@vlmdrounds hahah you’re definitely making progress! Next video you’ll make 30! 😀
Looking forward to future vids!
Much interesting. But you pretty much with all your explenations goes towards lowering of LDL particles with statins. Higher number more risk.
What's the evidence here? When people with low LDL particle numbers get problems pretty much just as often. So i am pretty sure the the body's way to handle damage are the key, and that certenly vary greatly in individuals! No doubt you know your subject, but somthing just does not add up with the particle nr teori
Appreciate your thoughts. I refer to this in Episode 45.
You have not addressed that ldl particle size affects the overall incidence of heart disease. A lipid subfraction can differentiate between pattern A and Pattern B. If you have a large count of LDLs in pattern A that is associated with a reduced incidence whereas a high number in pattern B is where the real danger is.
Try episode 22. I think it was covered there.
Small particles are slightly more atherogenic but both sizes can get lodged. In the end she is correct that total ApoB containing particle number is the most important factor along with reducing inflammation to the extent possible.
@@Seanonyoutube its sugar that makes them turn bad. Without ldls we would die. The higher the ldl count the lower mortality.
Cholesterol is not involved at all. One never sees atheromas in the venous side of the circulatory system, only in the arterial side. Cholesterol exists in the blood which travels in both sides.
The higher pressures on the arterial side result in more shear force flow with damage to the glycocalyx and lipoproteins entering the arterial wall. There are other differences between veinous and arterial blood. Intriguingly, there's a much higher % of lymphocytes (adaptive cells) in arterial blood vs. venous, which may impact the immune reactions in both.
@@vlmdrounds true which is why cholesterol is not the culprit as many still believe. However plz explain this ?
Atherosclerosis in vein grafts, It is a well-known clinical observation that veins used to replace arteries in coronary artery bypass grafts can develop atherosclerosis. This suggests that veins are capable of developing atherosclerosis under certain conditions. Why dr?
@@dombarton2483 Yes, happy to. I will explain in the next few episodes. This episode was just a general overview and I can go into some important points in the next ones. Thank you so much for listening.
@@vlmdrounds it is my pleasure. You provide such value and insight into all things medical. You are truly one of the elites!!